Influence of omega-3 supplementation in rats exposed to cigarette smoke associated with Induced Apical Periodontitis: bone and inflammatory analysis

Abstract

The development of apical periodontitis (PA) occurs after contamination of the root canal system triggering an inflammatory immune response and consequent periapical bone loss. Cigarette smoke is a complex mixture capable of acting on oral and systemic health. In periodontal disease, smoking is considered a significant risk factor, as it interferes with the supporting and protective periodontium, promoting inflammatory changes. To balance exacerbated inflammatory responses, Omega-3 fatty acids (É-3 PUFAs) have been used as adjunctive therapy in the treatment of systemic and oral diseases, due to their anti-inflammatory properties. The aim of this study will be to evaluate the influence of Omega-3 supplementation in Wistar rats exposed to cigarette smoke inhalation on induced apical periodontitis. Sixty-four animals will be divided into 8 groups (n=8): C (control, rats without PA and without cigarette exposure; PA (rats with induced apical periodontitis); F (rats exposed to cigarette smoke); FPA (rats with induced apical periodontitis and exposed to cigarette smoke); PA+O (rats with induced apical periodontitis supplemented with Omega-3); F+O (rats exposed to cigarette smoke supplemented with Omega-3); FPA+O (rats with induced apical periodontitis exposed to cigarette smoke supplemented with Omega-3), C+O (rats without PA without cigarette exposure supplemented with Omega-3) For inhalation of cigarette smoke, animals (F, FPA, F+ O, FPA+O) will be placed in a smoking chamber for eight minutes, three times a day for 20 days before BP induction. The same procedure will be performed in non-smoking animals (C, PA, C+O, PA+O ), but without the presence of cigarette smoke. On the 5th day of inhalation, the animals in the groups (C+O, PA+O, F+O, FPA+O) will start prophylactic supplementation a with Omega-3 for 15 days and the control animals (C, PA, F, FPA) will receive distilled water for the same period. On the 20th day, the animals will have the pulp of the first lower right molars exposed to the oral environment for the induction of the periapical lesion (PA), and will remain open for a period of 30 days. During this period, the animals will continue inhaling cigarette smoke associated with therapeutic supplementation for another 30 days, totaling 50 days of smoke inhalation protocol and 45 days of Omega-3 supplementation. At the time of euthanasia, blood will be collected for laboratory blood analysis and the jaws will be removed and processed for histopathological analysis of the severity of the inflammatory profile and bone resorption by staining in Hematoxylin and Eosin (HE) and Goldner's Trichomic (TG). Inflammatory (TNF-a, IL-6, IL-1b) and anti-inflammatory (IL-10) activity, as well as osteoclastogenesis (RANKL and OPG) using the immunohistochemical technique, and the volume of resorption will also be evaluated. bone by computerized microtomography analysis (Micro-CT) The data obtained will be tabulated and submitted to statistical analysis with a significance level of 5%. (AU)